Abstract
Atherosclerosis is the leading cause of death in the developed world. The build-up of atherosclerotic lesions within the arterial wall are responsible for life threatening events including stroke. The vascular wall is exposed to a number of stresses that require cellular responses to maintain homeostasis. The calcium/calmodulin-dependent protein kinase II (CaMKII) isoform family has important roles in maintaining vascular homeostasis but more recently emerged in the context of vascular dysfunction.
Previously, we showed that systemic inhibition of CaMKII leads to a reduction of atherosclerosis in the brachiocephalic artery of a mouse model of atherosclerosis (ApoE-/-). The next critical step in translating this work to a clinical intervention is to investigate which isoform of CaMKII contributes to atherogenesis.